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Acute stress disorder is used to help identify many individuals in the acute phase that will consequently develop chronic PTSD. The particular diagnostic criteria in acute stress disorder permit a more accurate identification of those who will not naturally recover from the adverse effects of their traumatic experience. After a traumatic event it is normal for people to constitute a psychological adaptation to a stressful event, limiting painful thoughts and feelings connected to the event allowing the person to minimal functioning. When these symptoms persist, they may impair the person’s quality of life and disrupt social and other functioning. If symptoms continue past a month after the event, PTSD may develop, continuing for months or even years after the precipitating event (Bryant, et al., 1999; Koopman, et al., 1995).
Not everyone who experience’s a traumatic event will develop acute stress disorder or PTSD. Those that become impaired ma have difficulty in the ability to vary anxiety levels in response to different situation. In the psychodynamic theory, Freud assumed that pathological anxiety resulted from a failure to repress painful memories, thoughts or impulses. However, the behavioral theory views conditioning as essential in perpetuating and intensifying anxiety. The biological theory also known as the James-Lange theory claimed, peripheral symptoms provoked central anxiety (Maxmen & Ward, 1995).
Symptoms and distress are common after a severe trauma and might represent a normative process. But by identifying the acute trauma phase in those who are at risk of developing chronic PTSD, provide an opportunity to prevent further development through early intervention. In a study (Bryant, Sackville, Dang, et al., 1998) of treatment to acute stress disorder, cognitive therapy was an effective technique for resolving acute trauma responses that would otherwise lead to chronic PTSD. In the cognitive process the belief is that resolution of a traumatic experience requires prolonged activation of trauma-related mental representations in order to allow habituation of anxiety and modification of maladaptive trauma-related belief. Chronic PTSD is mediated by deficits in accessing trauma memories during the acute trauma phase. Prolonged exposure also leads to longstanding gains in the treatment of chronic PTSD (Marshall, Spitzer, Liebowitz, 1999; Bryant, Sackville, Dang, et al., 1999).
Evidence has shown that acute stress reactions are mediated by elevated arousal. Anxiety management techniques can lead to significant reductions in PTSD symptoms. It is possible that habituation of anxiety through prolonged exposure and modification of maladaptive beliefs through cognitive therapy were the critical therapeutic processes that mediated adaptation. This information processing theory believes, recovery from trauma requires; activation of traumatic memories and modification of threat-based beliefs to correct the fear networks that perpetuate PTSD symptoms (Bryant, Sackville, Dang, et al., 1999).
Culturally endorsed rituals, psychological methods, such as, support and formal crisis intervention, focused psychotherapy, and psychopharmacology have a significant effect on the symptomatology of acute stress disorder. The biological models of PTSD suggest that excessive arousal at the time of the traumatic event results in strong fear conditioning that result in PTSD. Activation in the acute trauma phase may mediate PTSD because of limbic-based associations between the traumatic experience and heightened arousal. One study (Shaleu et al., 1998) reported heart rates of trauma survivors were higher in those that developed PTSD later. The development of PTSD is associated with reduced cortisol levels in the acute phase. Cortisol functions to control a series of biological reactions in the hypothalamic-pituitary-adrenal axis, lowering the cortisol contributes to elevated arousal (Lundin, 1994; Marshall, Spitzert, Liebowitz, 1999; Bryant, Sackville, Dang, et al., 1999; Bryant, Harvey, Guthrie, Moulds, 2000).
People with premorbid mood disorders other than major depression and premorbid axis I and axis II disorders have an increased risk in developing acute stress disorder. Many studies have shown dissociative symptoms correlate with high levels of anxiety and in PTSD symptoms (Mashall, Spitzer, Liebowtiz, 1999). Approximately 80% of people reporting derealization also report reduced awareness and depersonalization. This suggests the need for further studies on the operational understanding of dissociative symptoms in the acute trauma stage (Harvey, Bryant, 1999).
The biological affects are connected to the synaesthetic response, or as Damasio calls it, a somatic marker. The ‘feeling’ is about the body, this and mark images both are automated signals which focus our attention on the outcome to which a given action may lead. Somatic markers include both visceral and non-visceral input, whereas the synaesthetic response appears to depend on visceral input only (Damasio, 1994).
A somatic marker focuses on a negative outcome or highlights a good solution. It narrows the number of possible choices and the pause allows the person to decide which way to respond. The synaesthetic response is a special instance of background feelings. This background is monitored continuously. The somatic marker has a role in biological regulation. The archaic structures help classify things or events as good or bad because the consequences of achieving or not achieving a personal or social goal contribute to survival as well as the quality of that survival (Damasio, 1994).
Emotions are either primary or secondary. Primary are innate and preorganized. This depends mainly on the amygdala, limbic system circuitry and anterior cingulate. Humans are wired to respond with an emotion in a preorganized fashion when certain features of the stimuli are perceived. This is processed and then detected by a component of the brain’s limbic system that has a dispositional representation. This triggers a body state typical of an emotion, such as fear. It then alters cognitive processing to fit the state of fear (Damasio, 1994; Flannery, 1992).
The secondary emotion is acquired. The stimulus may still be processed directly via the amygdala but it is also analyzed in the thought processes and can activate the limbic system. The experience of an emotion can introduce significant changes in the acquired emotions that leads to chronic stress (Damasio, 1994)
Damasio states these changes are the result of; conscious, deliberate considerations about a person or situation; networks in the prefrontal cortex automatically and involuntarily respond to signals arising from the processing of the images; and the response of the prefrontal dispositional representations signaled to the amygdala and the anterior cingulate unconsciencely, automatically and involuntarily. These changes encroach upon the body, cause an emotional body state and are subsequently signaled back to the limbic and somatosensory systems. Emotion is the combination of a mental evaluative process, simple or complex, with dispositional responses to that process, mostly toward the body proper, resulting in an emotional body state, but also toward the brain itself, resulting in additional mental changes (Damasio, 1994).
Feelings are based on secondary emotions such as happiness, sadness, fear and anger. They correspond to profiles of preorganized body state responses. Somatic markers are a special instance of feelings generated from secondary emotions where the emotions and feelings are connected, by learning, to predicted future outcomes of certain scenarios in one’s personal life and its immediate social context (Damasio, 1994).
It is difficult to decide which develops first, the faulty cognitive processing or biological traits that may lead to the faulty thought process. Both appear to be integrated and should be treated in the same manner. Once the symptoms are controlled by cognitive methods, the biological symptoms will also begin to decrease. However, it may benefit the individual if the biological symptoms were addressed first, i.e., psychopharmacology, in order to allow cognitive reconstruction.
For references please e-mail me at: abinormal@qwest.net
